Alteration in immune complex glomerulonephritis by arachidonic acid.
We employed a model of immune complex glomerulonephritis produced in mice by the daily injection of apoferritin to study the effect of treatment with arachidonic acid (AA). Apoferritin injections produced demonstrable glomerular damage by light microscopy associated with deposition of immunoglobulin along peripheral capillary loops. Treatment with AA 100 micrograms daily resulted in significantly less glomerular damage and a shift inthe location of immune complex deposition to the mesangium. The amount of anti-apoferritin antibody was determined by hemagglutination and found to be significantly decreased in mice treated with AA. Separate studies employing this dose of AA revealed that the number of IgM antibody producing cells to SRBC was not altered by AA.
D000818:Animals; D000906:Antibodies / Q000032:analysis; D001052:Apoferritins / Q000276:immunology; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000627:therapeutic use*; D015232:Dinoprostone; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000139:chemically induced / Q000188:drug therapy*; D006386:Hemagglutination Tests; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D051379:Mice; D011458:Prostaglandins E / Q000652:urine; D010948:Viral Plaque Assay
D000906:Antibodies; D001095:Arachidonic Acids; D011458:Prostaglandins E; D016718:Arachidonic Acid; D001052:Apoferritins; D015232:Dinoprostone